Bcl-xL prevents apoptosis through two different mechanisms: heterodimerization with an apoptotic protein inhibits its apoptotic effect and formation of mitochondrial outer membrane pores help maintain a normal membrane state under stressful conditions. Bcl-xL is phosphorylated by JNK following treatment with microtubule-damaging agents, such as paclitaxel, vinblastine, and nocodazole.
